Journal of Alzheimer's Disease - Volume 3, issue 1

Authors: Selkoe, Dennis J.

Article Type: Research Article

DOI: 10.3233/JAD-2001-3111

Citation: Journal of Alzheimer's Disease, vol. 3, no. 1, pp. 75-80, 2001

Authors: Masters, Colin L. | Beyreuther, Konrad

Article Type: Research Article

DOI: 10.3233/JAD-2001-3112

Citation: Journal of Alzheimer's Disease, vol. 3, no. 1, pp. 83-86, 2001

Authors: Gambetti, Pierluigi | Parchi, Piero | Capellari, Sabina | Russo, Claudio | Tabaton, Massimo | Teller, Jan K. | Chen, Shu G.

Article Type: Research Article

DOI: 10.3233/JAD-2001-3113

Citation: Journal of Alzheimer's Disease, vol. 3, no. 1, pp. 87-95, 2001

Authors: Nixon, Ralph A. | Mathews, Paul M. | Cataldo, Anne M.

Article Type: Research Article

Abstract: Robust activation of the neuronal lysosomal system and cellular pathways converging on the lysosome, such as the endocytic and autophagic pathways, are prominent neuropathological features of Alzheimer's disease. Disturbances of the neuronal endocytic pathway, which are one of the earliest known intracellular changes occurring in Alzheimer's disease and Down syndrome, provide insight into how ß-amyloidogenesis might be promoted in sporadic Alzheimer's disease, the most prevalent and least well understood form of the disease. Primary lysosomal system dysfunction in inherited disorders is commonly associated with prominent neurological phenotypes and neurodegeneration. New studies now directly implicate lysosomal cathepsins as proteases capable of …initiating, as well as executing, cell death programs. These and other studies support the view that the progressive alterations of lysosomal system function in Alzheimer's disease have broad relevance to the neurodegenerative processes occurring during the disease. Show more

DOI: 10.3233/JAD-2001-3114

Citation: Journal of Alzheimer's Disease, vol. 3, no. 1, pp. 97-107, 2001

Authors: Hardy, John

Article Type: Research Article

Abstract: With the application of molecular genetics, we are now beginning to understand the etiology and the early stages of pathogenesis of the major neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Pick's disease and Progressive Supranuclear Palsy. Surprisingly, these studies are showing that these diseases share pathogenic mechanisms which involve tau or synuclein aggregation. In this article, I review the progress in the molecular genetic analysis of these major neurodegenerative diseases and discuss how they are related to each other.

DOI: 10.3233/JAD-2001-3115

Citation: Journal of Alzheimer's Disease, vol. 3, no. 1, pp. 109-116, 2001

Authors: Trojanowski, John Q. | Lee, Virginia M.-Y.

Article Type: Research Article

DOI: 10.3233/JAD-2001-3116

Citation: Journal of Alzheimer's Disease, vol. 3, no. 1, pp. 117-119, 2001

Authors: Masliah, Eliezer

Article Type: Research Article

Abstract: Synaptic damage is an early pathological event common to many neurodegenerative disorders such as Alzheimer's disease (AD) and is the best correlate to the cognitive impairment. Several molecules involved in AD and in other neurodegenerative disorders play an important role in synaptic function and when misfolded aggregate and form amyloid fibrils. Synaptic proteins with an amyloid domain include amyloid ß-protein precursor, prion protein, huntingtin, ataxin-1 and α-synuclein. Two of the possible mechanisms by which alterations in synaptic proteins lead to synapse damage are: 1) misfolded or aggregated synaptic molecules have lost their normal function and/or 2) they have gained a …toxic capacity. Recent studies support the possibility that while oligomers are toxic, polymers might be inactive. The mechanisms by which oligomers trigger synapse loss could be related to their ability to triggers stress signals once they enter the nucleus and/or accumulate at the endoplasmic reticulum. Show more

DOI: 10.3233/JAD-2001-3117

Citation: Journal of Alzheimer's Disease, vol. 3, no. 1, pp. 121-129, 2001

Authors: Strohmeyer, Ron | Rogers, Joseph

Article Type: Research Article

DOI: 10.3233/JAD-2001-3118

Citation: Journal of Alzheimer's Disease, vol. 3, no. 1, pp. 131-157, 2001